Abstract
Murphy argues that deletion of β-catenin in macrophages is a caveat to our interpretation that Wnt signaling programs dendritic cells (DCs) into a tolerogenic state in the gut. However, our data demonstrate that β-catenin–deficient DCs are greatly impaired in inducing regulatory T cells, and induce enhanced T helper 17 (T H 17)/T H 1 responses. Assessing the relative importance of DCs versus macrophages in intestinal tolerance must await tools that permit the genetic deletion of the numerous DC and macrophage subsets in the intestine.
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